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Biomedical subjects

P G Tremml

Publications and source records attributed to P G Tremml.

6 recordsLinked to original sources
PubMed1989

Effect of thermal conditions on the acceptability of respiratory protective devices on humans at rest.

The physiological and subjective responses of six sedentary subjects wearing half-facepiece respirators were observed over a wide range of room and respirator air conditions. Room air and dew-point (Ta:Tdp) temperatures were 25:11 degrees, 30:13 degrees, and 35:16 degrees C in still air. Respirator air temperatures were maintained independently of room conditions at 27 degrees, 30 degrees, 33 degrees, and 36 degrees C with relative humidity levels of 47% and 73%. Physiological measurements included local skin and dew-point temperatures. Subjective judgments of acceptability, thermal sensation, degree of discomfort, sense of skin moisture, and difficulty of breathing were recorded separately for the thermal environment in the room and inside the respirator. Respirator temperatures cooler than 33 degrees C were always comfortable and 100% acceptable; respirator air temperatures above 33 degrees C or higher humidity levels decreased respirator acceptability. Acceptability of the respirator environment decreased as lip temperature increased above 34.5 degrees C or when respirator dew-point temperature increased above 20 degrees C. Increased respirator air temperature and humidity often made breathing seem "slightly hard." The respirator conditions influenced the subjects' judgment of the acceptability of the surrounding thermal environment.

Adult↗
PubMed1988

Pressor and hemodilution responses compensate for acute hemorrhage in bluefish.

1. After hemorrhage of 21% blood volume (0.9% body weight) blood pressure (BP) and heart rate (H.R.) of unanesthetized bluefish (Pomatomus saltatrix) recovered within 5 min. 2. Phentolamine blocked this recovery. 3. Atropine increased control H.R. from 48 to 87 per min, and to 108 after hemorrhage, with delay of BP recovery to 10 min. 4. With small, repeated hemorrhages every 20 min, hemodilution and recovery of BP occurred between hemorrhages. Removal of 27% blood volume resulted in only temporary recovery. 5. Thirty min after hemorrhage, plasma epinephrine was 5 x and norepinephrine 8 x control. 6. Thus, bluefish tolerate hemorrhage with initial vasoconstriction via alpha-adrenergic pathways, and hemodilution.

Animals↗
PubMed1988

Airway responsiveness and prostaglandin generation in scorbutic guinea pigs.

Airway responsiveness to histamine aerosol and lung prostaglandin generation were investigated in normal, partially vitamin C deficient and scorbutic guinea pigs. The ascorbic acid content of the lung expressed as microgram/100 mg wet weight lung parenchyma decreased from 22.1 +/- 1.8 (mean +/- SE) in the control group to 9.0 +/- 1.4 and 1.8 +/- 0.4 in tissues from partially ascorbic acid deficient and scorbutic animals, respectively. Guinea pigs on low and ascorbic acid deficient diets developed significant airway hyperresponsiveness to histamine aerosol after 3 and 4 weeks. Indomethacin (30 mg/Kg, i.p.) further increased the airway hyperresponsiveness in scorbutic animals but was without effect in control animals. Prostaglandin generation from different parts of the lung was significantly changed by the diets. However, airway hyperresponsiveness was not directly attributable to altered prostanoid generation. Scorbutic conditions did not alter the electrophysiological characteristics of airway smooth muscle namely, resting membrane potential and electrogenic sodium pump activity. In summary, ascorbic acid deficiency causes airway hyperresponsiveness to histamine in guinea pigs. This alteration seems not to be related to an altered prostaglandin generation by the lung or to the electrophysiological properties of airway smooth muscle.

Aerosols↗
PubMed1986

Ascorbic acid promotes prostanoid release in human lung parenchyma.

Ascorbic acid reduces airway reactivity to inhaled bronchoconstrictor agents in man and guinea pigs. The precise mechanism(s) responsible for this effect are unknown, but in both species an acute indomethacin treatment reverses the action of the ascorbic acid. To determine if ascorbic acid promotes prostanoid synthesis and/or inhibits degradation, human lung parenchymal slices (100-200 mg) were incubated for 60 minutes in oxygenated Tyrode's solution alone or with sodium ascorbate (0.001 M-1 M) and/or methacholine (1 microM-100 microM) and/or indomethacin (0.17 microM-17 microM). Aliquots of the incubation medium were assayed by radioimmunoassay for PGE2, PGF2 alpha, thromboxane B2 and 6-keto-PGF1 alpha. Ascorbic acid increased the accumulation of all four prostanoids in the incubation medium, especially thromboxane B2 and 6-keto-PGF1 alpha. This stimulatory effect of ascorbic acid was concentration-dependent and was inhibited by indomethacin. We conclude that ascorbic acid can alter prostanoid generation by human lung tissue and this effect may, in part, explain its antibronchoconstrictor activity in man.

Ascorbic Acid↗
PubMed1986

Colloid osmotic pressure changes in human whole blood and separated plasma in vitro with changes in CO2 content and pH.

Colloid osmotic pressure (COP) and pH were measured on the true plasma of human blood from five subjects tonometered with different concentrations of carbon dioxide. Measurements were also made on their separated plasma. COP (mmHg) of true plasma obtained from tonometered whole blood varied in proportion to the bicarbonate concentration (mEq/l): COP = 0.056 [HCO3-] + 23.3. In separated plasma, as CO2 concentration increased, COP decreased as pH decreased: COP = 1.99 (pH) + 11.0. When the change in COP due to the change in pH was subtracted from the observed change of COP due to CO2 exposure of whole blood, the difference was the change of COP due to the shift of fluid between plasma and red cells: COP adjusted for pH = 0.131 [HCO3-] + 21.5. The COP values of tonometered whole blood and separated plasma are taken to be equal at a pH of 7.40 (at the mixed venous point). The change in COP, adjusted for pH, for a given change in pCO2 is in keeping with the amount of fluid shift calculated from the measured changes in hematocrit and plasma protein concentration. An error in a previous paper (Kakiuchi et al., J. appl. Physiol. 44, 474-478, 1978) had led to an overestimation of the COP change from the exposure of whole blood to CO2 in vitro.

Blood Physiological Phenomena↗